Since atherosclerotic coronary heart disease is the single greatest cause of death in the United States, the need to provide a means to prevent myocardial infarction or to at least reduce the size of any infarct after a coronary occlusion occurs has resulted in considerable investigation. Attempts to increase the supply of blood to the heart by means of a coronary vasodilator in order to prevent the onset of myocardial infarction have not only been unsuccessful but have actually been found to be contraindicated. Thus, it has been found that the administration of the common vasodilators such as nitroglycerin after the occurrence of a coronary occlusion causes increased work of the heart, edema and an increase in blood pressure, all of which result in a worsening of the subsequent myocardial infarction.
As a consequence, present medical practice in the case of the occurrence of a coronary occlusion is to simply have the patient rest, to treat the pain, for example with morphine, and sometimes to administer a vasopressor, namely dopamine. No drug treatment has been established to prevent or reduce the size of myocardial infarction.